A reinforcement learning based decision support system in textile manufacturing process

This paper introduced a reinforcement learning based decision support system in textile manufacturing process. A solution optimization problem of color fading ozonation is discussed and set up as a Markov Decision Process (MDP) in terms of tuple {S, A, P, R}. Q-learning is used to train an agent in the interaction with the setup environment by accumulating the reward R. According to the application result, it is found that the proposed MDP model has well expressed the optimization problem of textile manufacturing process discussed in this paper, therefore the use of reinforcement learning to support decision making in this sector is conducted and proven that is applicable with promising prospects

Modeling Color Fading Ozonation of Textile Using Artificial Intelligence

International audienceTextile products with faded effect achieved via ozonation are increasingly popular recently. In this study, the effect of ozonation in terms of pH, temperature, water pickup , time and applied colors on the color fading performance of reactive-dyed cotton are modeled using Extreme Learning Machine (ELM), Support Vector Regression (SVR) and Random Forest Regression (RF) respectively. It is found that RF and SVR perform better than ELM in this issue, but SVR is more recommended to be sued in the real application due to its balance predicting performance and less training time

Interferon-α regulates glutaminase 1 promoter through STAT1 phosphorylation: relevance to HIV-1 associated neurocognitive disorders.

HIV-1 associated neurocognitive disorders (HAND) develop during progressive HIV-1 infection and affect up to 50% of infected individuals. Activated microglia and macrophages are critical cell populations that are involved in the pathogenesis of HAND, which is specifically related to the production and release of various soluble neurotoxic factors including glutamate. In the central nervous system (CNS), glutamate is typically derived from glutamine by mitochondrial enzyme glutaminase. Our previous study has shown that glutaminase is upregulated in HIV-1 infected monocyte-derived-macrophages (MDM) and microglia. However, how HIV-1 leads to glutaminase upregulation, or how glutaminase expression is regulated in general, remains unclear. In this study, using a dual-luciferase reporter assay system, we demonstrated that interferon (IFN) α specifically activated the glutaminase 1 (GLS1) promoter. Furthermore, IFN-α treatment increased signal transducer and activator of transcription 1 (STAT1) phosphorylation and glutaminase mRNA and protein levels. IFN-α stimulation of GLS1 promoter activity correlated to STAT1 phosphorylation and was reduced by fludarabine, a chemical that inhibits STAT1 phosphorylation. Interestingly, STAT1 was found to directly bind to the GLS1 promoter in MDM, an effect that was dependent on STAT1 phosphorylation and significantly enhanced by IFN-α treatment. More importantly, HIV-1 infection increased STAT1 phosphorylation and STAT1 binding to the GLS1 promoter, which was associated with increased glutamate levels. The clinical relevance of these findings was further corroborated with investigation of post-mortem brain tissues. The glutaminase C (GAC, one isoform of GLS1) mRNA levels in HIV associated-dementia (HAD) individuals correlate with STAT1 (

Serial deletion reveals structural basis and stability for the core enzyme activity of human glutaminase 1 isoforms: relevance to excitotoxic neurodegeneration.

BACKGROUND: Glutaminase 1 is a phosphate-activated metabolic enzyme that catalyzes the first step of glutaminolysis, which converts glutamine into glutamate. Glutamate is the major neurotransmitter of excitatory synapses, executing important physiological functions in the central nervous system. There are two isoforms of glutaminase 1, KGA and GAC, both of which are generated through alternative splicing from the same gene. KGA and GAC both transcribe 1-14 exons in the N-terminal, but each has its unique C-terminal in the coding sequence. We have previously identified that KGA and GAC are differentially regulated during inflammatory stimulation and HIV infection. Furthermore, glutaminase 1 has been linked to brain diseases such as amyotrophic lateral sclerosis, Alzheimer\u27s disease, and hepatic encephalopathy. Core enzyme structure of KGA and GAC has been published recently. However, how other coding sequences affect their functional enzyme activity remains unclear. METHODS: We cloned and performed serial deletions of human full-length KGA and GAC from the N-terminal and the C-terminal at an interval of approximately 100 amino acids (AAs). Prokaryotic expressions of the mutant glutaminase 1 protein and a glutaminase enzyme activity assay were used to determine if KGA and GAC have similar efficiency and efficacy to convert glutamine into glutamate. RESULTS: When 110 AAs or 218 AAs were deleted from the N-terminal or when the unique portions of KGA and GAC that are beyond the 550 AA were deleted from the C-terminal, KGA and GAC retained enzyme activity comparable to the full length proteins. In contrast, deletion of 310 AAs or more from N-terminal or deletion of 450 AAs or more from C-terminal resulted in complete loss of enzyme activity for KGA/GAC. Consistently, when both N- and C-terminal of the KGA and GAC were removed, creating a truncated protein that expressed the central 219 AA - 550 AA, the protein retained enzyme activity. Furthermore, expression of the core 219 AA - 550 AA coding sequence in cells increased extracellular glutamate concentrations to levels comparable to those of full-length KGA and GAC expressions, suggesting that the core enzyme activity of the protein lies within the central 219 AA - 550 AA. Full-length KGA and GAC retained enzyme activities when kept at 4 °C. In contrast, 219 AA - 550 AA truncated protein lost glutaminase activities more readily compared with full-length KGA and GAC, suggesting that the N-terminal and C-terminal coding regions are required for the stability KGA and GAC. CONCLUSIONS: Glutaminase isoforms KGA and GAC have similar efficacy to catalyze the conversion of glutamine to glutamate. The core enzyme activity of glutaminase 1 protein is within the central 219 AA - 550 AA. The N-terminal and C-terminal coding regions of KGA and GAC help maintain the long-term activities of the enzymes

AMPK Signaling in Energy Control, Cartilage Biology, and Osteoarthritis

The adenosine monophosphate (AMP)–activated protein kinase (AMPK) was initially identified as an enzyme acting as an “energy sensor” in maintaining energy homeostasis via serine/threonine phosphorylation when low cellular adenosine triphosphate (ATP) level was sensed. AMPK participates in catabolic and anabolic processes at the molecular and cellular levels and is involved in appetite-regulating circuit in the hypothalamus. AMPK signaling also modulates energy metabolism in organs such as adipose tissue, brain, muscle, and heart, which are highly dependent on energy consumption via adjusting the AMP/ADP:ATP ratio. In clinics, biguanides and thiazolidinediones are prescribed to patients with metabolic disorders through activating AMPK signaling and inhibiting complex I in the mitochondria, leading to a reduction in mitochondrial respiration and elevated ATP production. The role of AMPK in mediating skeletal development and related diseases remains obscure. In this review, in addition to discuss the emerging advances of AMPK studies in energy control, we will also illustrate current discoveries of AMPK in chondrocyte homeostasis, osteoarthritis (OA) development, and the signaling interaction of AMPK with other pathways, such as mTOR (mechanistic target of rapamycin), Wnt, and NF-κB (nuclear factor κB) under OA condition

Ultralow-emittance measurement of high-quality electron beams from a laser wakefield accelerator

By designing a cascaded laser wakefield accelerator, high-quality monoenergetic electron beams (e beams) with peak energies of 340–360MeV and rms divergence of <0.3 mrad were produced. Based on this accelerator, the e-beam betatron radiation spectra were measured exactly via the single-photon counting technique to diagnose the e-beam transverse emittance in a single shot. The e-beam transverse size in the wakefield was estimated to be ~0.35 lm by comparing the measured X-ray spectra with the analytical model of synchrotron-like radiation. By combining the measured e-beam energy and divergence, the normalized transverse emittance was estimated to be as low as 56 um mrad and consistent with particle-in-cell simulations. These high-energy ultralow-emittance e beams hold great potential applications in developing free electron lasers and high-energy X-ray and gamma ray sources

Enhanced betatron radiation by steering a laser-driven plasma wakefield with a tilted shock front

We have experimentally realized a scheme to enhance betatron radiation by manipulating transverse oscillation of electrons in a laser-driven plasma wakefield with a tilted shock front (TSF). Very brilliant betatron x-rays have been produced with significant enhancement both in photon yield and peak energy but almost maintain the e-beam energy spread and charge. Particle-in-cell simulations indicate that the accelerated electron beam (e beam) can acquire a very large transverse oscillation amplitude with an increase in more than 10-fold, after being steered into the deflected wakefield due to the refraction of the driving laser at the TSF. Spectral broadening of betatron radiation can be suppressed owing to the small variation in the peak energy of the low-energy-spread e beam in a plasma wiggler regime. It is demonstrated that the e-beam generation, refracting, and wiggling can act as a whole to realize the concurrence of monoenergetic e beams and bright x-rays in a compact laser-wakefield accelerator

Interferon-α Regulates Glutaminase 1 Promoter through STAT1 Phosphorylation: Relevance to HIV-1 Associated Neurocognitive Disorders

HIV-1 associated neurocognitive disorders (HAND) develop during progressive HIV-1 infection and affect up to 50% of infected individuals. Activated microglia and macrophages are critical cell populations that are involved in the pathogenesis of HAND, which is specifically related to the production and release of various soluble neurotoxic factors including glutamate. In the central nervous system (CNS), glutamate is typically derived from glutamine by mitochondrial enzyme glutaminase. Our previous study has shown that glutaminase is upregulated in HIV-1 infected monocyte-derived-macrophages (MDM) and microglia. However, how HIV-1 leads to glutaminase upregulation, or how glutaminase expression is regulated in general, remains unclear. In this study, using a dual-luciferase reporter assay system, we demonstrated that interferon (IFN) α specifically activated the glutaminase 1 (GLS1) promoter. Furthermore, IFN-α treatment increased signal transducer and activator of transcription 1 (STAT1) phosphorylation and glutaminase mRNA and protein levels. IFN-α stimulation of GLS1 promoter activity correlated to STAT1 phosphorylation and was reduced by fludarabine, a chemical that inhibits STAT1 phosphorylation. Interestingly, STAT1 was found to directly bind to the GLS1 promoter in MDM, an effect that was dependent on STAT1 phosphorylation and significantly enhanced by IFN-α treatment. More importantly, HIV-1 infection increased STAT1 phosphorylation and STAT1 binding to the GLS1 promoter, which was associated with increased glutamate levels. The clinical relevance of these findings was further corroborated with investigation of post-mortem brain tissues. The glutaminase C (GAC, one isoform of GLS1) mRNA levels in HIV associated-dementia (HAD) individuals correlate with STAT1 (p<0.01), IFN-α (p<0.05) and IFN-β (p<0.01). Together, these data indicate that both HIV-1 infection and IFN-α treatment increase glutaminase expression through STAT1 phosphorylation and by binding to the GLS1 promoter. Since glutaminase is a potential component of elevated glutamate production during the pathogenesis of HAND, our data will help to identify additional therapeutic targets for the treatment of HAND

Layer-controlled synthesis of graphene-like MoS \u3c inf\u3e 2 from single source organometallic precursor for Li-ion batteries

Herein, we report an new approach to synthesis of graphene-like MoS 2 flakes and tunable layers (from mono- to multi-layer) easily controlled by the thermal decomposition temperature of a single source (Mo(Et2NCS2)4). The approach opens a new way to controlled large-scalable synthesis of graphene-like transition metal sulfides for energy storage, nanoelectronics and optoelectronics. © 2014 the Partner Organisations